Article
Inhalation injury to tracheal epithelium in an ovine model of cotton smoke exposure. Early phase (30 minutes).
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.
The American review of respiratory disease (impact factor:
10.19).
01/1991;
142(6 Pt 1):1436-9.
pp.1436-9
Source: PubMed
-
Citations (0)
- Cited In (2)
-
Article: Cell adhesion molecules and the bronchial epithelium.
[show abstract] [hide abstract]
ABSTRACT: The bronchial epithelium is the major barrier between the host and the provoking antigens in bronchial asthma. Recent studies have indicated that the epithelium is a truly stratified structure, with the superficial columnar cells depending on the underlying basal cells for anchorage. Only columnar cells are shed into bronchial lavage fluid. The epithelium is more fragile in asthma and more cells are lost in clusters. Desmosomes appear to be the major structural adhesion mechanism at the plane of cleavage between the columnar cells and the basal cells. The alpha 6- and beta 4-integrins, which contribute to hemidesmosomes and anchor cells to the underlying basement membrane, are expressed solely by basal cells. The apical aspects of the columnar cells are sealed by tight and intermediate junctions. There is constitutive expression of ICAM-1 and E-selectin in the vasculature of the bronchial mucosa, and ICAM is also present within the epithelium. These findings indicate that the bronchial epithelium is a complex structure that, as a mucosal surface, has constitutive expression of inflammatory cell adhesion molecules to serve normal leukocyte traffic.The American review of respiratory disease 01/1994; 148(6 Pt 2):S79-82. · 10.19 Impact Factor -
Article: Inflammatory mediators in smoke inhalation injury.
[show abstract] [hide abstract]
ABSTRACT: Smoke inhalation occurs in 10% to 30% of patients admitted to burn centers, and increases mortality by a maximum of 20% over that predicted by age and extent of cutaneous burn alone. Pneumonia in these patients then further increases mortality by a maximum of 40%. While one estimate suggested that 75% of deaths following burn injury may be accounted for by inhalation injury, more recent cohort studies have suggested there is a decreasing mortality attributable to inhalation injury. As part of understanding and improving outcomes from burn injuries, the pathophysiology and inflammatory processes involved in smoke inhalation injury has been extensively investigated in animal models. This review will emphasize the inflammatory pathways involved in inhalation injury, and targeted methods used to treat this injury in both experimental and human models.Inflammation & allergy drug targets. 04/2009; 8(1):63-9.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed.
The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual
current impact factor.
Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence
agreement may be applicable.
Keywords
apical cell surface
basal cells
cells desmosomal attachment
Ciliated cells
cotton smoke
endotracheal intubation
epithelial surface
extruding mucus
first experiment 5 sheep
following number
goblet cells
modified bee smoker
Numerous ciliated cells
remaining ciliated cells
sham group
sloughed cells
smoke breaths
smoke inhalation injury
transmission electron
vesiculated cytoplasm